BACKGROUND & AIMS: Unexplained dyspeptic symptoms are associated with changes in gastric sensorimotor function and several psychopathologic dimensions, including anxiety. It is unclear whether this reflects common predisposition or a causal relationship. The aim of this study was to investigate whether experimentally induced anxiety would alter gastric sensorimotor function in health. METHODS: Fourteen subjects underwent a gastric barostat study to assess gastric sensitivity and accommodation. Eighteen subjects underwent a 10-minute satiety drinking test (30 mL/min) with registration of epigastric symptoms on a visual analogue scale (VAS) at 2-minute intervals. Emotional context was modulated for 10 minutes at the start of each experiment by combined projection of validated facial expressions and an audiotape recalling a neutral or an anxious autobiographical experience. Anxiety levels were assessed using a VAS and the Spielberger State-Trait Anxiety Inventory (STAI). RESULTS: VAS and STAI scores confirmed efficacy of anxiety induction. During the anxiety condition, gastric compliance was significantly decreased (57 +/- 5 vs 40 +/- 5 mL/mm Hg; P < .01). Intraballoon pressures inducing discomfort during gastric distention were not altered, but the corresponding volume (630 +/- 47 vs 489 +/- 39 mL; P < .005) was significantly lower. Meal-induced relaxation was inhibited during the anxiety condition and this persisted for the 60-minute measurement (157 +/- 29 vs 100 +/- 24 mL; P < .05). During the satiety drinking test, the anxiety condition was associated with significantly higher scores for satiety, fullness, and bloating. CONCLUSIONS: Experimentally induced anxiety alters gastric sensorimotor function, suggesting that psychological factors may play a causal role in the pathogenesis of some dyspeptic symptoms and mechanisms.
BACKGROUND & AIMS: Unexplained dyspeptic symptoms are associated with changes in gastric sensorimotor function and several psychopathologic dimensions, including anxiety. It is unclear whether this reflects common predisposition or a causal relationship. The aim of this study was to investigate whether experimentally induced anxiety would alter gastric sensorimotor function in health. METHODS: Fourteen subjects underwent a gastric barostat study to assess gastric sensitivity and accommodation. Eighteen subjects underwent a 10-minute satiety drinking test (30 mL/min) with registration of epigastric symptoms on a visual analogue scale (VAS) at 2-minute intervals. Emotional context was modulated for 10 minutes at the start of each experiment by combined projection of validated facial expressions and an audiotape recalling a neutral or an anxious autobiographical experience. Anxiety levels were assessed using a VAS and the Spielberger State-Trait Anxiety Inventory (STAI). RESULTS: VAS and STAI scores confirmed efficacy of anxiety induction. During the anxiety condition, gastric compliance was significantly decreased (57 +/- 5 vs 40 +/- 5 mL/mm Hg; P < .01). Intraballoon pressures inducing discomfort during gastric distention were not altered, but the corresponding volume (630 +/- 47 vs 489 +/- 39 mL; P < .005) was significantly lower. Meal-induced relaxation was inhibited during the anxiety condition and this persisted for the 60-minute measurement (157 +/- 29 vs 100 +/- 24 mL; P < .05). During the satiety drinking test, the anxiety condition was associated with significantly higher scores for satiety, fullness, and bloating. CONCLUSIONS: Experimentally induced anxiety alters gastric sensorimotor function, suggesting that psychological factors may play a causal role in the pathogenesis of some dyspeptic symptoms and mechanisms.
Authors: I J Llewellyn-Smith; D O Kellett; D Jordan; K N Browning; R Alberto Travagli Journal: Neurogastroenterol Motil Date: 2011-12-21 Impact factor: 3.598
Authors: C N Andrews; A E Bharucha; M Camilleri; P A Low; B M Seide; D D Burton; K K Nickander; K L Baxter; A R Zinsmeister Journal: Neurogastroenterol Motil Date: 2007-09 Impact factor: 3.598